Stress-induced suppression of pulsatile luteinising hormone release in thefemale rat: Role of vasopressin

Insulin-induced hypoglycaemic (IIH) stress evokes the release of arginine v asopressin (AVP) and suppresses luteinising hormone (LH) pulses in a number of species, a phenomenon augmented by the presence of oestradiol (E-2). Th e aim of this study was to test the hypothesis that AVP not only disrupts p ulsatile LH secretion in the female rat, but specifically mediates the effe ct of IIH stress on suppressing LH release. The role of E-2 in augmenting t he disruptive effect of AVP on LH secretion was also addressed. Rats were o variectomized (OVX) and fitted with intracerebroventricular (i.c.v.) and in travenous (i.v.) cannulae. For experiments requiring comparisons of neuroen docrine responses in the presence and absence of E-2, animals were implante d subcutaneously with E-2 or oil-filled capsules respectively. AVP (5 mu g) administered via the i.c.v. cannula suppressed LH secretion by decreasing LH pulse amplitude without affecting LH pulse frequency, an effect that was blocked by central administration of an AVP antagonist (25 mu g) This inhi bitory response was evident only in E-2-replaced OVX rats, thus suggesting a sensitizing influence of the gonadal steroid. In the AVP-deficient Brattl eboro rats, IIH stress did not interrupt pulsatile LH secretion as demonstr ated in Long Evans and Wistar controls. While these data might suggest a pi votal role for AVP in stress-induced suppression of LH release, central adm inistration of an AVP antagonist did not prevent the interruption of LH pul ses in response to IIH stress. Furthermore, it would appear that AVP is not primarily involved in hypoglycaemic stress-induced suppression of pulsatil e LH secretion since central administration of very high doses of AVP resul ted in a suppression of LH pulse amplitude and not frequency, while hypogly caemic stress caused an interruption of LH pulses.